Myasthenia Gravis: It's Diagonosis And Treatment

4268 words - 17 pages

MYASTHENIA GRAVIS, IT ‘s DIAGONOSIS AND TREATMENT
Myasthenia gravis [MG] is a rare, autoimmune neuromuscular disorder. The incidence rates has been reported as 2-7/10000 in central and western Virginia ( Thanvi ,2004).The onset of [MG] is depends on age and gender .In patients younger than 40 years, women are more susceptible than man to [MG],with a ratio of 7:3 :Above the age 50 [MG] are slightly more common in men with a ratio 3:2.Myasthenia gravis are very rare in children.Juvinile [MG] is an autoimmune disorder ,while congenital [MG] results from genetic mutations that impair neuromuscular transmission. It has been suggested that incidence of [MG] falls after 70 years of age. A recent study using AChR antibody as a diagnostic tool, has shown that myasthenia gravis was considerably under –diagnosed in people >75 years in the UK
The branching terminus of a nerve cell of α-motor neuron axons from the ventral horns of the spinal cord and brainstem provides the nerve terminals that form the neuro-muscular junction (figure 1).The myelinated axons reach the muscles through peripheral nerves ;then each axon separates into branches that innervate many individual muscle fibres (Gardener,1968). As it approaches its target fibre each branch loses the myelin sheath and further subdivides into many presynaptic knobs, which are composed of synaptic vesicles loaded with ACh and face the side of synaptic cleft. The presynaptic knob and postsynaptic knob are separated by the synaptic cleft, a space that contains acetyl cholinesterase (AChE) and other proteins and proteoglycans involved in stabilizing the neuro-muscular junction. The postsynaptic knob has some deep infolds and, possess acetylcholine receptors (AChRs) (Bianca et al 20006).
In myasthenia gravis, a disorder characterised by muscular weakness and rapid tiring of muscles, the activity between acetylcholine and it’s receptor is prevented by antibodies in the serum .The anti-bodies bind to Ach receptors and cause a destruction of the tips of folds of the muscle membrane where the receptors are concentrated (David, 1983).Subsequent damage to postsynaptic membrane results in simplification of normal, highly infolded surface that is accompanied by reduced number of acetylcholine receptors. The functional loss of AChRs reduces the probability of successful neuromuscular transmission following adequate release of acetylcholine by the motor nerve terminal (Gardener,1968).The relationship between myasthenia gravis and thymoma was noted more than 200 years ago,thymic abnormalities are found in nearly 75% of patients with myasthenia gravis.Of these ,germinal hyperplasia is noted in 85% and thymic tumours in 15%.Antistriated muscle antibodies are present in 90% of patients with myasthenia gravis and athymoma (B Thanvi and lo ,2004).
The following figures 1 and 2 display what exactly happens at the postsynaptic membrane when affected by [MG].

Figure 1.The cleft space is small compared ...

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